A miodarone, an effective iodine-rich antiarrhythmic drug, frequently causes either changes in thyroid function tests or clinical thyroid dysfunction. Both amiodarone-induced THYROTOXICOSIS (AIT) and amiodarone-induced hypothyroidism (AIH) have an overall incidence of approximately 14- 18%, and AIT being most common in iodinedeficient areas, AIH in iodine-sufficient areas. Both dysfunctions may develop either in apparently normal thyroid glands or in glands with preexisting abnormalities (either nodular goiter or thyroid autoimmune disease). The most important pathogenic mechanisms of AIT include excess iodine-induced thyroid hormone synthesis (type I AIT) and amiodarone (or iodine) - related destructive thyroiditis (type II AIT), but mixed forms involving both pathogenic mechanisms are likely more frequent than previously believed. AIT is a therapeutic challenge, because rapid restoration of euthyroidism is warranted in patients with underlying cardiac disorders. Treatment of choice for type I AIT is represented by the concomitant administration of thionamides and potassium perchlorate, whereas steroids are the most useful tool for type II AIT. Mixed (or, better, undefined) forms of AIT should be treated with a combination of thionamides, potassium perchlorate and glucocorticoids. Radioiodine therapy is usually not feasible owing to low thyroidal radioiodine uptake due to iodine load, while thyroidectomy can be performed in cases resistant to medical therapy or in those patients requiring a rapid control of THYROTOXICOSIS after a short course with iopanoic acid to restore normal serum T3 levels. Thyroid ablation is usually required in type I and undefined AIT, also because this allows safe reinstitution of amiodarone treatment, if needed; follow-up without treatment is sufficient in most patients with type II AIT, who usually remain euthyroid or may develop hypothyroidism after reexposure to iodine load.

Background and objective-In THYROTOXICOSIS, changes in urine output and serum creatinine (Cr) concentration has been related to increased glomerular filtration rate (GFR). The aim of this study is to clarify the mechanism of these changes. Methods-Forty-one thyrotoxic patients, 9 male and 32 female with the age range of 16-62 years were selected and body weight, 24-h urine output, serum and urine Cr concentration, and GFR were measured in the thyrotoxic state and two months after treatment. The data was analyzed by student ‘t’ test and paired ‘t’ test. Results-The following parameters were measured and are compared in thyrotoxic and euthyroid states respectively. Body weight: 58.4±10.6 Kg and 61.6±10.4 Kg after receiving anti-thyroid therapy (p<0.001). 24-h urine output: 1430±420 ml, and 1165±450 ml (p <0.001). Serum creatinine concentration: 0.7±0.11 mg/dl, and 0.84±0.13 mg/dl (p<0.001). 24-h urine creatinine concentration: 906±225 mg/l and 1081±285 mg/l (p<0.001). The change in GFR was not statistically significant, being 90.1 ml/min before therapy and 89.5 ml/min in the euthyroid state. Conclusion-Increased urine output and decreased serum creatinine concentration in THYROTOXICOSIS is not GFR related.

Background: Insulin resistance and abnormal glucose metabolism are the main characteristics of THYROTOXICOSIS and gestational diabetes mellitus (GDM). However, it remains unclear whether THYROTOXICOSIS increases the risk of GDM. Therefore, this research aimed to explore the causality between THYROTOXICOSIS and GDM by using a Mendelian randomization (MR) analysis. Methods: A MR analysis was conducted to explore the causal effects of THYROTOXICOSIS on GDM. Summary statistics data of THYROTOXICOSIS (3115 THYROTOXICOSIS cases and 187684 controls) and GDM (13039 cases and 197831 controls) were derived from genome-wide association study. We selected MR Egger, Weighted median, Inverse-variance weighted, Simple mode and Weighted mode to evaluate the causal effect between THYROTOXICOSIS and GDM. Results: By using a two-sample MR analysis, we found a strong causal relationship between THYROTOXICOSIS and GDM as indicated by Inverse-variance weighted (OR=1.069; beta=0.067; 95%CI=1.023-1.118; P=0.003), Weighted median (OR=1.087; beta=0.084; 95%CI=1.040-1.137; P=0.0002), Simple mode (OR=1.102; beta=0.097; 95%CI= 1.038-1.170; P=0.013) and Weighted mode (OR=1.089; beta=0.085; 95%CI=1.033-1.147; P=0.013). No significant pleiotropy, heterogeneity, genetic correlations or bi-directional causal relationship was existed in this study. Bayesian colocalization suggested that THYROTOXICOSIS colocalized with GDM on rs10830963 (PP.H4 = 1.000), where rs10830963 was located on MTNR1B gene locus. Conclusion: THYROTOXICOSIS had a causal effect on the risk of developing GDM, and the exposure of THYROTOXICOSIS increased the risk of GDM.

Context: THYROTOXICOSIS may be associated with a better sense of well-being than in the euthyroid state, though this is not widely recognised. Evidence Acquisition: A comprehensive literature search in PubMed and Google Scholar, was performed to identify studies investigating factors influencing well-being, mood, and psychological features associated with elevated thyroid hormones. Results: Enhanced well-being associated with THYROTOXICOSIS has been described, although the evidence is observational and anecdotal. Conclusions: Enhancedwell-being associated with THYROTOXICOSIS is probably experiencedin a minority of patientsandmayexplain why some seek overtreatment with thyroid hormones and report significant improvement on larger than physiological thyroid hormone replacement regimens. It may also explain why some patients with hyperthyroidism (usually due to Graves’ disease) are reluctant to adhere to anti-thyroid medication.